Nogapendekin alfa (his tag)
Based on 1 Customer Validation
Nogapendekin alfa his tag is an immunostimulant that binds to the IL-2RβγC complex on immune cells. Nogapendekin alfa his tag stimulates the proliferation and activation of natural killer cells and CD8+ T cells, upregulates the expression of granzyme B and perforin, and activates the innate and adaptive immune branches. Nogapendekin alfa his tag forms ALT-803 with IL-15RαSuFc; this complex has an extended biological half-life, improved biodistribution and retention in lymphoid tissues, enhances natural killer cell-mediated rituximab-dependent cellular cytotoxicity, and reduces tumor burden and improves survival when combined with anti-CD20 monoclonal antibody therapy. Nogapendekin alfa his tag can be used in the research of non-Hodgkin's lymphoma.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 純度 : 98.62%
- CAS 番号: 1622189-43-8
- 分子量:13.91 kDa
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保管条件:Shipping with dry ice
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
Species Reactivity
Human
IC50 & Target
[1]|
IL-2RβγC |
IL-15RαSuFc |
体外実験
Nogapendekin alfa his tag (48 h), when fused to the sc2B8 anti-CD20 single-chain antibody as part of the 2B8T2M complex, retains IL-15 biological activity supporting 32Dβ cell proliferation with an EC50 of 889 pM, though at reduced potency compared to native IL-15 and ALT-803[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
体内実験
Nogapendekin alfa his tag (1 mg per instillation; intravesical; weekly; 6 weeks) reduces NMIBC tumor burden by 35% in rats, with enhanced efficacy (46% tumor burden reduction, 76% angiogenesis reduction, 80% proliferation reduction) when combined with intravesical BCG, mediated by increased tumoral immune cell infiltration[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J mice (orthotopic non-muscle-invasive bladder cancer induced via BBN)[1]
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Dosage:0.2 mg/kg (s.c. single-agent); 0.1 mg per instillation (intravesical single-agent); 0.2 mg/kg (s.c.) plus 135 mg per instillation intravesical BCG; 0.1 mg per instillation (intravesical) plus 135 mg per instillation intravesical BCG
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Administration:s.c.; weekly; 6 weeks; intravesical; weekly; 6 weeks
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Result:Reduced tumor burden by 37%, a greater reduction than intravesical administration (28%) or intravesical BCG alone (28%).
Reduced tumor burden by 44% when combined with intravesical BCG, while intravesical administration combined with intravesical BCG reduced tumor burden by 36%.
Increased populations of peripheral CD8+ T, NK (NKG2D+), NKT (CD3+/NKG2D+), and splenic NKT cells, whereas intravesical administration alone and intravesical BCG alone did not affect these lymphocyte populations.
Increased serum IL-5 and IL-6 levels and urine IL-13 levels to a greater extent than intravesical BCG.
Reduced serum IL-1β levels alone or in combination with intravesical BCG.
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Animal Model:C57BL/6J mice (healthy)[1]
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Dosage:0.2 mg/kg (s.c., single dose); 0.2 mg/kg (i.v., single dose); 1.0 mg/kg (s.c., weekly for 4 weeks)
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Administration:s.c.; single dose; i.v.; single dose; s.c.; weekly; 4 weeks
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Result:Increased serum levels of IL-6, IFNγ, MCP-1, granzyme B (GzB), and TNFα, without altering IL-10 or IL-12 levels.
Promoted IFNγ and TNFα secretion in splenocytes, without changing IL-6, IL-2, IL-10, IL-4, or IL-17A levels.
Increased spleen weight and counts of CD8+ T cells and NK cells, with effects on CD8+ T, Treg, and NK cell proliferation in the spleen, and GzB upregulation, similar to intravenous administration.
Increased spleen weight by 5.5-fold, lymph node weight by threefold, and liver weight by approximately 0.2-fold.
Increased counts of white blood cells (ninefold), lymphocytes (ninefold), neutrophils (eightfold), monocytes (sevenfold), eosinophils (sixfold), and basophils (fourfold).
Reduced blood alkaline phosphatase (ALP) and creatinine levels without affecting hepatotoxicity or nephrotoxicity markers.
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Animal Model:Sprague-Dawley (SD) rats (orthotopic non-muscle-invasive bladder cancer induced via BBN)[1]
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Dosage:1 μg per instillation (intravesical single-agent); 1 mg per instillation (intravesical) plus 135 mg per instillation intravesical BCG
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Administration:intravesical; weekly; 6 weeks
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Result:Reduced tumor burden by 35%, tumor angiogenesis by 59%, and tumor cell proliferation by 52%.
Reduced tumor burden by 46%, tumor angiogenesis by 76%, and tumor cell proliferation by 80%, outperforming intravesical BCG alone (15% tumor burden reduction, 40% angiogenesis reduction, 40% proliferation reduction).
Increased tumoral CD3+ T cell counts to a greater extent than intravesical BCG alone; the combination further enhanced tumoral NK cell counts compared to either agent alone.
Stimulated secretion of IL-1α, IL-1β, and RANTES to enhance NK cell proliferation and activation.
Conjugated
Unconjugated
Reconstitution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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IL15 (interleukin 15, IL-15)variant N72>D
アプリケーション
ELISA, FACS, Functional assay
化学情報
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CAS 番号 1622189-43-8
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性状 Liquid
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分子量 13.91 kDa
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Color Colorless to light yellow
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SMILES
[Nogapendekin alfa (his tag)]
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別名
IL-15N72D
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輸送条件
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
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データシート (258 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Inhibitory Antibodies User Guide (603 KB)
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)